Low temperature protects mammalian cells from apoptosis initiated by various stimuli in vitro

Sakurai, Toshiharu; Itoh, Katsuhiko; Liu, Yu; Higashitsuji, Hiroaki; Sumitomo, Yasuhiko; Sakamaki, Kazuhiro; Fujita, Jun

doi:10.1016/j.yexcr.2005.06.002

Cited by 50 publications

(38 citation statements)

References 39 publications

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“…Protection from cell death under conditions of mild hypothermia (32-35°C) has been extensively studied in neurons and has been used therapeutically for neuronal cytoprotection after brain injury (15). Lowering temperature has also been reported to delay apoptosis in other cell types, including cardiomyocytes and fibroblasts, and diverse mechanisms have been implicated, but previous studies have not specifically addressed epithelial cells (16,17). Therefore, we next examined whether temperature dependence of cell death tracked with a particular apoptotic pathway by treating cells with known triggers of extrinsic and intrinsic apoptosis.…”

Section: Resultsmentioning

confidence: 99%

Two interferon-independent double-stranded RNA-induced host defense strategies suppress the common cold virus at warm temperature

Foxman

Storer

Vanaja

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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Most strains of rhinovirus (RV), the common cold virus, replicate better at cool temperatures found in the nasal cavity (33-35°C) than at lung temperature (37°C). Recent studies found that although 37°C temperature suppressed RV growth largely by engaging the type 1 IFN response in infected epithelial cells, a significant temperature dependence to viral replication remained in cells devoid of IFN induction or signaling. To gain insight into IFN-independent mechanisms limiting RV replication at 37°C, we studied RV infection in human bronchial epithelial cells and H1-HeLa cells. During the single replication cycle, RV exhibited temperature-dependent replication in both cell types in the absence of IFN induction. At 37°C, earlier signs of apoptosis in RV-infected cells were accompanied by reduced virus production. Furthermore, apoptosis of epithelial cells was enhanced at 37°C in response to diverse stimuli. Dynamic mathematical modeling and B cell lymphoma 2 (BCL2) overexpression revealed that temperature-dependent host cell death could partially account for the temperature-dependent growth observed during RV amplification, but also suggested additional mechanisms of virus control. In search of a redundant antiviral pathway, we identified a role for the RNA-degrading enzyme RNAseL. Simultaneous antagonism of apoptosis and RNAseL increased viral replication and dramatically reduced temperature dependence. These findings reveal two IFN-independent mechanisms active in innate defense against RV, and demonstrate that even in the absence of IFNs, temperature-dependent RV amplification is largely a result of host cell antiviral restriction mechanisms operating more effectively at 37°C than at 33°C. apoptosis | RNaseL | innate immunity | rhinovirus | respiratory immunity I n the 1960s, rhinoviruses (RVs) were first cultured from patient samples and shown to cause acute upper respiratory infections (a.k.a. common colds). Early work showed that RV isolates replicated best in culture when incubated at temperatures slightly cooler than core body temperature (33-35°C) (1, 2). This observation fit with the role of RV as a cause of disease in the nasal cavity, but not the lungs, as the nasal cavity is cooled by inhalation of environmental air, but the lungs are generally considered to be at core body temperature (37°C). The primary target cells of RV infection are the airway epithelial cells that line the respiratory tract. Similar to all cells of the body, airway epithelial cells are equipped with a cell-intrinsic innate immune system that can sense the presence of a viral infection, using pattern recognition receptors such as toll-like receptors (TLRs) and RIG-I like receptors (RLRs), and can respond to the infection by inducing antiviral effector mechanisms (3). Recently, we used mouse primary airway cells and a mouse-adapted RV to show that replicating RV is recognized by the RLRs within airway epithelial cells, leading to two innate immune signaling events that occur more robustly at warm temperature than at cool temperatu...

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Section: Resultsmentioning

confidence: 99%

Two interferon-independent double-stranded RNA-induced host defense strategies suppress the common cold virus at warm temperature

Foxman

Storer

Vanaja

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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“…27). Mammalian cells exposed to a variety of cytotoxic and apoptotic stimuli were rescued by hypothermia (32°C), and this suppression was mediated partly through caspase-9-dependent and p53-dependent and -independent mechanisms (52). Similarly, apoptosis through the caspase-3-dependent pathway was attenuated in cardiomyocytes from hypothermia-treated rats in response to hemorrhagic shock compared with normothermic rats (56).…”

Section: C399mentioning

confidence: 99%

Enhanced survival of skeletal muscle myoblasts in response to overexpression of cold shock protein RBM3

Ferry

Vanderklish

Dupont‐Versteegden

2011

American Journal of Physiology-Cell Physiology

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Ferry AL, Vanderklish PW, Dupont-Versteegden EE. Enhanced survival of skeletal muscle myoblasts in response to overexpression of cold shock protein RBM3. Am J Physiol Cell Physiol 301: C392-C402, 2011. First published May 18, 2011; doi:10.1152/ajpcell.00098.2011 is suggested to be involved in the regulation of skeletal muscle mass. Cell death pathways are implicated in the loss of muscle mass and therefore the role of RBM3 in muscle apoptosis in C 2C12 myoblasts was investigated in this study. RBM3 overexpression was induced by either cold shock (32°C exposure for 6 h) or transient transfection with a myc-tagged RBM3 expression vector. Cell death was induced by H 2O2 (1,000 M) or staurosporine (StSp, 5 M), and it was shown that cold shock and RBM3 transfection were associated with attenuation of morphological changes and an increase in cell viability compared with normal temperature or empty vector, respectively. No changes in proliferation were observed with either cold shock or RBM3 transfection. DNA fragmentation was not increased in response to H 2O2, and a cell permeability assay indicated that cell death in response to H 2O2 is more similar to necrosis than apoptosis. RBM3 overexpression reduced apoptosis and the collapse of the membrane potential in response to StSp. Moreover, the increase in caspase-3, -8, and -9 activities in response to StSp was returned to control levels with RBM3 overexpression. These results indicate that increased RBM3 expression decreases muscle cell necrosis as well as apoptosis and therefore RBM3 could potentially serve as an intervention for the loss of muscle cell viability during muscle atrophy and muscle diseases. muscle atrophy; hibernation; RNA-binding proteins; apoptosis; necrosis SKELETAL MUSCLE HAS A REMARKABLE capacity to adapt to changes in mechanical and metabolic environment. Whereas increased use in the form of resistance exercise leads to hypertrophy, reduced muscle activity, as well as certain physiological and pathological processes, can lead to a severe loss in muscle mass (for review see Ref. 25). Skeletal muscle atrophy is often associated with diseases such as cancer, acquired immunodeficiency syndrome, diabetes, and congestive heart failure, and when present carries a poor prognosis (6, 44). In addition, age-related loss of muscle mass (sarcopenia) is an important predictor of mortality in the aged (40,48,49,63) and has been suggested as a main contributor to the loss of independence in elderly (40, 50). Muscle atrophy is also a common symptom in neuromuscular diseases, even though the etiology of the disorders is often quite different. Cell deathrelated signaling events are common in muscle cells undergoing atrophy, but the exact role of apoptosis, autophagy, and necrosis (three common forms of cell death) remains to be determined.In a previous study, we identified the cold-inducible RNAbinding motif protein 3 (RBM3) as a possible regulator of skeletal muscle mass under disuse-induced atrophy (23). RBM3 gene expression and protein abundance were increased ...

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“…apoptosis (Rincon and Mayer 2006). Apoptosis is principally mediated through caspase-8 or caspase-9 activating pathway and DNA damage associated apoptosis requires activation of the p53 gene (Sakurai et al 2005). In vitro studies have shown that hypothermia selectively protects cells from these mediators of cell death (Sakurai et al 2005).…”

Section: Intra-arrest Coolingmentioning

confidence: 99%

“…Apoptosis is principally mediated through caspase-8 or caspase-9 activating pathway and DNA damage associated apoptosis requires activation of the p53 gene (Sakurai et al 2005). In vitro studies have shown that hypothermia selectively protects cells from these mediators of cell death (Sakurai et al 2005). Bearing this and the fact that hypothermia increases tissue tolerance to hypoxia (Alzaga et al 2006;Rosomoff and Holaday 1954) in mind, it is tempting to pursue the beneficial effects of induced hypothermia already during the ischaemic insult, as currently done during cardiac and neurosurgery, in association with cardiac arrest.…”

Section: Intra-arrest Coolingmentioning

confidence: 99%

Pre‐hospital cardiac arrest and induction of mild hypothermia: studies on epidemiology and feasibility

Kämäräinen¹

2010

Acta Anaesthesiol Scand

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Low temperature protects mammalian cells from apoptosis initiated by various stimuli in vitro

Cited by 50 publications

References 39 publications

Two interferon-independent double-stranded RNA-induced host defense strategies suppress the common cold virus at warm temperature

Two interferon-independent double-stranded RNA-induced host defense strategies suppress the common cold virus at warm temperature

Enhanced survival of skeletal muscle myoblasts in response to overexpression of cold shock protein RBM3

Pre‐hospital cardiac arrest and induction of mild hypothermia: studies on epidemiology and feasibility

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